Mitragyna speciosa Korth. downregulates macrophage inflammatory responses by inhibiting TLR-4 and increasing IL-10 production

Anwar Salm Kalifa Kafo; Rabia Mrehil Elsalami; Masriana Hassan

Makale detayları

Mitragyna speciosa Korth. downregulates macrophage inflammatory responses by inhibiting TLR-4 and increasing IL-10 production

Yazarlar:

Anwar Salm Kalifa Kafo | Rabia Mrehil Elsalami | Masriana Hassan

Yayıncı:

Istanbul University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

İstanbul Journal of Pharmacy Vol.54 Issue 3, pp.350-358

Belge Tipi:

Makale

Yayın Tarihi:

12/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001340662

pISSN:

2587-2087

Anahtar kelimeler:

Özet:

 Background and Aims: Mitragyna speciosa Korth. is a tropical plant native to Asia with various medicinal properties. This study examined the immunotherapeutic potential of M. speciosa methanolic extract MSME against lipopolysaccharide LPS- stimulated activation of macrophages via the expression of Toll-like receptor 4 TLR-4 and CD14 and downstream signalling cascades leading to the activation of nuclear factor kappa B NF-B, which potentially affects macrophage immune responses. Methods: The expression of TLR-4CD14 and NF-B genes in macrophages was determined in total RNA by qRT-PCR. Subsequently, the macrophage phagocytic activities and secretion of immune mediators such as reactive oxygen species ROS and cytokines were evaluated by fluorescent latex beads uptake assay, 2,7-dichlorodihydrofluorescein diacetate H2DCFDA, and cytometric bead array, respectively, in LPS-activated RAW264.7 cells. Results: MSME significantly reduced macrophage-mediating inflammation by inhibiting TLR-4CD14 signalling and subsequently suppressed the NF-B expression. Inhibition of TLR-4 by MSME attenuated macrophage phagocytic activity, which consequently reduced the production of ROS and pro-inflammatory cytokines such as IL-6, MCP-1, and TNF-α. Interestingly, MSME significantly increased the production of IL-10, which supports the anti-inflammatory properties of M. speciosa. Conclusion: Our findings suggest the therapeutic potential of MSME through the suppression of macrophage inflammatory responses mediated by IL-10 secretion.

 Background and Aims: Mitragyna speciosa Korth. is a tropical plant native to Asia with various medicinal properties. This study examined the immunotherapeutic potential of M. speciosa methanolic extract MSME against lipopolysaccharide LPS- stimulated activation of macrophages via the expression of Toll-like receptor 4 TLR-4 and CD14 and downstream signalling cascades leading to the activation of nuclear factor kappa B NF-B, which potentially affects macrophage immune responses. Methods: The expression of TLR-4CD14 and NF-B genes in macrophages was determined in total RNA by qRT-PCR. Subsequently, the macrophage phagocytic activities and secretion of immune mediators such as reactive oxygen species ROS and cytokines were evaluated by fluorescent latex beads uptake assay, 2,7-dichlorodihydrofluorescein diacetate H2DCFDA, and cytometric bead array, respectively, in LPS-activated RAW264.7 cells. Results: MSME significantly reduced macrophage-mediating inflammation by inhibiting TLR-4CD14 signalling and subsequently suppressed the NF-B expression. Inhibition of TLR-4 by MSME attenuated macrophage phagocytic activity, which consequently reduced the production of ROS and pro-inflammatory cytokines such as IL-6, MCP-1, and TNF-α. Interestingly, MSME significantly increased the production of IL-10, which supports the anti-inflammatory properties of M. speciosa. Conclusion: Our findings suggest the therapeutic potential of MSME through the suppression of macrophage inflammatory responses mediated by IL-10 secretion.

 Background and Aims: Mitragyna speciosa Korth. is a tropical plant native to Asia with various medicinal properties. This study examined the immunotherapeutic potential of M. speciosa methanolic extract MSME against lipopolysaccharide LPS- stimulated activation of macrophages via the expression of Toll-like receptor 4 TLR-4 and CD14 and downstream signalling cascades leading to the activation of nuclear factor kappa B NF-B, which potentially affects macrophage immune responses. Methods: The expression of TLR-4CD14 and NF-B genes in macrophages was determined in total RNA by qRT-PCR. Subsequently, the macrophage phagocytic activities and secretion of immune mediators such as reactive oxygen species ROS and cytokines were evaluated by fluorescent latex beads uptake assay, 2,7-dichlorodihydrofluorescein diacetate H2DCFDA, and cytometric bead array, respectively, in LPS-activated RAW264.7 cells. Results: MSME significantly reduced macrophage-mediating inflammation by inhibiting TLR-4CD14 signalling and subsequently suppressed the NF-B expression. Inhibition of TLR-4 by MSME attenuated macrophage phagocytic activity, which consequently reduced the production of ROS and pro-inflammatory cytokines such as IL-6, MCP-1, and TNF-α. Interestingly, MSME significantly increased the production of IL-10, which supports the anti-inflammatory properties of M. speciosa. Conclusion: Our findings suggest the therapeutic potential of MSME through the suppression of macrophage inflammatory responses mediated by IL-10 secretion.

 Background and Aims: Mitragyna speciosa Korth. is a tropical plant native to Asia with various medicinal properties. This study examined the immunotherapeutic potential of M. speciosa methanolic extract MSME against lipopolysaccharide LPS- stimulated activation of macrophages via the expression of Toll-like receptor 4 TLR-4 and CD14 and downstream signalling cascades leading to the activation of nuclear factor kappa B NF-B, which potentially affects macrophage immune responses. Methods: The expression of TLR-4CD14 and NF-B genes in macrophages was determined in total RNA by qRT-PCR. Subsequently, the macrophage phagocytic activities and secretion of immune mediators such as reactive oxygen species ROS and cytokines were evaluated by fluorescent latex beads uptake assay, 2,7-dichlorodihydrofluorescein diacetate H2DCFDA, and cytometric bead array, respectively, in LPS-activated RAW264.7 cells. Results: MSME significantly reduced macrophage-mediating inflammation by inhibiting TLR-4CD14 signalling and subsequently suppressed the NF-B expression. Inhibition of TLR-4 by MSME attenuated macrophage phagocytic activity, which consequently reduced the production of ROS and pro-inflammatory cytokines such as IL-6, MCP-1, and TNF-α. Interestingly, MSME significantly increased the production of IL-10, which supports the anti-inflammatory properties of M. speciosa. Conclusion: Our findings suggest the therapeutic potential of MSME through the suppression of macrophage inflammatory responses mediated by IL-10 secretion.

Makale detayları

Mitragyna speciosa Korth. downregulates macrophage inflammatory responses by inhibiting TLR-4 and increasing IL-10 production

Yazarlar:

Anwar Salm Kalifa Kafo | Rabia Mrehil Elsalami | Masriana Hassan

Yayıncı:

Istanbul University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

İstanbul Journal of Pharmacy Vol.54 Issue 3, pp.350-358

Belge Tipi:

Makale

Yayın Tarihi:

12/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001340662

pISSN:

2587-2087

Mitragyna speciosa

Macrophages; Anti-inflammatory

IL-10

TLR-4

Sayı

Makale detayları

Mitragyna speciosa Korth. downregulates macrophage inflammatory responses by inhibiting TLR-4 and increasing IL-10 production

Yazarlar: Anwar Salm Kalifa Kafo | Rabia Mrehil Elsalami | Masriana Hassan

Yayıncı: Istanbul University

Ana Başlıklar: Pharmacology and Pharmaceutical Sciences (Other)

Dergi: İstanbul Journal of Pharmacy Vol.54 Issue 3, pp.350-358

Belge Tipi: Makale

Yayın Tarihi: 12/2024

Belge Dili: İngilizce

Document ID (Org No.): 2001340662

pISSN: 2587-2087

Mitragyna speciosa

Macrophages; Anti-inflammatory

IL-10

TLR-4

Sayı

Yazarlar:

Anwar Salm Kalifa Kafo | Rabia Mrehil Elsalami | Masriana Hassan

Yayıncı:

Istanbul University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

İstanbul Journal of Pharmacy Vol.54 Issue 3, pp.350-358

Belge Tipi:

Makale

Yayın Tarihi:

12/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001340662

pISSN:

2587-2087